Thirty Fourth Installment

November 2025 Case Study

Robin Picavia, MD¹

1. Department of Dermatology, George Washington University School of Medicine and Health Sciences

Patient History 

A 52-year-old man presents with 2 weeks of fever, bilateral ankle swelling, and painful erythematous nodules on his shins. He reports a month of fatigue, decreased appetite, and 10-lb weight loss. Examination shows tender red subcutaneous nodules on the anterior lower legs and swelling of both ankles. Labs show an elevated ESR. Chest CT demonstrates bilateral hilar lymphadenopathy with mediastinal adenopathy and a small right upper lobe nodule. Biopsy of a shin lesion is consistent with erythema nodosum. 

Question:

Which of the following is the most likely diagnosis?

A. Löfgren syndrome
B. Polyarteritis nodosa
C. Erdheim–Chester disease
D. Erythema induratum (nodular vasculitis)
E. Sweet syndrome

Correct Answer: A. Löfgren syndrome

Explanation/Literature review:
Löfgren syndrome (Answer A) is an acute, self-limited presentation of sarcoidosis characterized by the classic triad of erythema nodosum, bilateral hilar lymphadenopathy, and acute
symmetric polyarthritis, most commonly involving the ankles. 1 Patients typically present with fever, malaise, and fatigue, often accompanied by weight loss and night sweats. 1 The arthritis is usually abrupt in onset, tender, and may be associated with periarticular inflammation or ankle swelling. Erythema nodosum appears as tender, erythematous nodules on the anterior shins and represents a reactive septal panniculitis rather than granulomatous skin disease. Chest imaging reveals bilateral hilar and right paratracheal lymphadenopathy; parenchymal lung involvement is less common in the acute setting. 1 Laboratory findings may include elevated ESR/CRP, mild leukocytosis or lymphopenia and occasionally elevated liver enzymes.

Importantly, Löfgren syndrome is associated with an excellent prognosis, with spontaneous remission in up to 80–90% of patients within 6–12 months. Treatment is often supportive, including NSAIDs for arthralgia, while short courses of corticosteroids may be used in more severe cases; long-term immunosuppression is rarely needed. Because the triad is highly specific, tissue biopsy is not always required unless atypical features or alternative diagnoses are suspected. 1

Polyarteritis nodosa (Answer B) is unlikely since it is a medium vessel necrotizing vasculitis that presents with livedo reticularis, neuropathy, renal involvement, and systemic symptoms but does not produce septal panniculitis or bilateral hilar lymphadenopathy. 2 Erdheim-Chester disease (Answer C) typically manifests with long-bone sclerosis, retroperitoneal fibrosis, orbital infiltration, and foamy histiocytic infiltrates, none of which fit this patient's biopsy-proven erythema nodosum or acute ankle arthritis; it also does not present with the sarcoidosis triad. 3

Erythema induratum (Answer D) involves lobular panniculitis with vasculitis, often associated with tuberculosis, and usually presents with tender nodules on the posterior calves rather than anterior shin lesions, making it inconsistent with this patient's clinical and histologic findings. 4

Sweet syndrome (Answer E) presents with acute tender plaques and a dense neutrophilic infiltrate on biopsy rather than septal panniculitis and does not produce bilateral hilar
lymphadenopathy, further excluding it from consideration. 5 Taken together, the clinical features and biopsy results most strongly support acute sarcoidosis consistent with Lofgren
syndrome.

References
1. Haimovic, A., Sanchez, M., Judson, M. A., & Prystowsky, S. (2012). Sarcoidosis: A
comprehensive review and update for the dermatologist. Journal of the American
Academy of Dermatology, 66(5), 699.e1–699.e18.
2. Stewart, M., & Mohan, N. (2022). Cutaneous polyarteritis nodosa diagnosis and
treatment: A retrospective case series. Journal of the American Academy of
Dermatology, 87(6), 1370–1373.
3. Maredia, H., et al. (2024). Atypical cutaneous manifestation of Erdheim–Chester disease
successfully treated using medical and laser therapy. JAAD Case Reports, 64, 75–78.
4. Gilchrist, H. and Patterson, J.W. (2010), Erythema nodosum and erythema induratum
(nodular vasculitis): diagnosis and management. Dermatologic Therapy, 23: 320-327.
https://doi.org/10.1111/j.1529-8019.2010.01332.x
5. Heath, M. S., & Ortega-Loayza, A. G. (2015). Erythema nodosum and other
panniculitides: Classification and approach. Journal of the American Academy of
Dermatology, 73(5), 691-705.

September 2025 Case Study

Caroline Clark, MD¹

1. Department of Dermatology, George Washington University School of Medicine and Health Sciences

Patient History

A 69-year-old male with a history of hypertension, rheumatoid arthritis, and HIV (recent viral load undetectable), presents in dermatology clinic with purplish discoloration around both eyes/upper cheeks which he states developed around 1 month ago (figure 1).  He endorses vague upper extremity muscle pain, but otherwise review of systems is negative. A punch biopsy was performed which vacuolar interface dermatitis with dermal mucin deposition.

Question:

Next, appropriate bloodwork is performed and reveals this patient has an elevated creatine kinase and positive Anti-TIF1-γ antibodies. What is the next best step in management?

1. Age-appropriate colonoscopy screening
2. Age-appropriate cancer screening + whole body PET scan
3. Muscle biopsy
4. High resolution chest CT scan
5. Start therapy with IVIG

Answer: 2.  Age-appropriate cancer screening + whole body PET scan

Explanation/Literature review:

Dermatomyositis (DM) is an idiopathic inflammatory myopathy characterized by progressive, symmetric, proximal muscle weakness and an array of distinct cutaneous manifestations.  Classic skin findings include a heliotrope rash, periorbital edema, red or violet papules overlying the bony prominences on the dorsal hands and other joints, such as the elbows and knees (Gottron papules), red-purple rash on the upper chest (V-sign), upper back, shoulders, and neck (shawl sign), or on the lateral hips and upper thighs (holster sign), and characteristic nail findings.^1,2

Initial workup for DM includes a detailed history and full body skin examination, baseline laboratory testing with muscle enzymes (creatine kinase, aldolase) and autoantibody testing.  A muscle biopsy may be indicated but should be reserved for equivocal cases in which diagnosis is unclear (Answer 3).

DM is associated with an increased prevalence of malignancy. Cancer risk is highest within a year of diagnosis and remains elevated for around 5 years.¹ Certain myositis-specific autoantibodies (MSAs) are present in about 20% of patients with DM.² MSAs are associated with varying degrees of malignancy risk and, if positive, can help guide appropriate management of cancer screenings. Anti-transcription intermediary factor 1 gamma (anti-TIF1- γ) and anti-nuclear matrix protein 2 (anti-NXP2) antibodies are both associated with high risk for DM-associated malignancy.¹ Individuals who are positive for either of these antibodies should undergo both age-appropriate cancer screening in addition to whole body imaging with either CT, MRI or PET (Answer 2).¹ Adult patients with DM who are negative for both anti-TIF1- γ and anti-NXP2 have a lower risk of malignancy associated DM and do not require additional cancer workup outside of standard age-based cancer screening, as more invasive cancer screening is unlikely to improve outcomes (Answer 1).

In all DM patients, regardless of antibody status, there should be a low threshold to undergo standard screening with pulmonary function testing (PFTs) and DLCO. Anti-melanoma differentiation-associated protein 5 (MDA5) antibody-positive DM is associated with increased risk for rapidly progressive interstitial lung disease (ILD). Patients positive for this antibody, or those with concerning respiratory symptoms, warrant additional workup with high-resolution CT scan (Answer 4) and pulmonology referral.³

While IVIG (Answer 5) is among the treatments available for DM, this is traditionally not initiated as a first-line therapy and cancer screening is the first priority in this patient.²

References:

1. Waldman R, DeWane ME, Lu J. Dermatomyositis: Diagnosis and treatment. J Am Acad Dermatol. 2020 Feb;82(2):283-296. doi: 10.1016/j.jaad.2019.05.105. Epub 2019 Jul 4. PMID: 31279813.
2. Cobos GA, Femia A, Vleugels RA. Dermatomyositis: An Update on Diagnosis and Treatment. Am J Clin Dermatol. 2020 Jun;21(3):339-353. doi: 10.1007/s40257-020-00502-6. PMID: 32096127.
3. Lu X, Peng Q, Wang G. Anti-MDA5 antibody-positive dermatomyositis: pathogenesis and clinical progress. Nat Rev Rheumatol. 2024 Jan;20(1):48-62. doi: 10.1038/s41584-023-01054-9. Epub 2023 Dec 6. PMID: 38057474.

August 2025 Case Study

Savanna Vidal, BS¹, Nagasai Adusumilli, MD, MBA^1
1Department of Dermatology, The George Washington University School of Medicine and Health Sciences

Patient History  

A gentleman in his 60s with PMH of HIV (CD4 178 on antiretroviral therapy), Hep C, Hep B, HTN, and prediabetes, was admitted for hypoglycemia and hypothermia after being found down. Dermatology was consulted for a diffuse pruritic, burning rash on the trunk and extremities for about 6 months. Medium potency topical corticosteroids provided partial relief of symptoms, but the patient described increasing number of pruritic plaques. Medication review showed amlodipine, lisinopril, trimethoprim/sulfamethoxazole, and metformin for his chronic medical conditions. Figures 1 and 2 demonstrate the pertinent skin findings.

Which of the following best describes the expected histopathology findings?

1. Compact orthokeratosis, lichenoid interface dermatitis, jagged rete ridges, eosinophilic remnants of keratinocytes in the epidermis
2. Dermis with marked inflammatory infiltrate of plasma cells around adnexal structures and vessels, irregular vascular spaces, hemosiderin deposition, and vessels wrapping pre-existing vessels
3. Lichenoid interface dermatitis with lymphocytic infiltrate deeper in the dermis, dermal melanin incontinence
4. Thin basket weave stratum corneum, vacuolar interface dermatitis with eosinophils and neutrophils, pigment incontinence in the papillary dermis
5. Neutrophils throughout the upper epidermis, with periodic acid–Schiff positive staining in the stratum corneum

Correct Answer: D

Explanation/Literature Review

With a CD4 count less than 200, this patient was newly taking trimethoprim/sulfamethoxazole for prophylaxis against pneumocystis pneumonia (PCP). The multiple, sharply demarcated, mostly circular and ovoid, thin, pigmented, pruritic plaques are most consistent with fixed drug eruption likely secondary to trimethoprim/sulfamethoxazole. The characteristic histopathology findings for fixed drug eruption include the mismatch of an acute stratum corneum and the chronic changes of the superficial dermis. The interface dermatitis is more vacuolar rather than lichenoid with a diffuse band of inflammation obscuring the dermal-epidermal junction. Eosinophils and pigment incontinence are commonly seen (Choice D).¹ The histopathologic findings can be similar to erythema multiforme and graft-versus-host disease. However, both histopathologic differential diagnoses will typically have more necrotic keratinocytes.¹

While theoretically any medication can cause a fixed drug eruption, trimethoprim/sulfamethoxazole is a classic offender estimated to encompass the majority of cases.² In addition to the clinical morphology, dermatologists must be aware of common contexts for which classic offending medications may be prescribed. Tetracyclines are often implicated for fixed drug eruption on the penis, and pseudoephedrine is a common cause of the nonpigmented variant.² After the initial exposure, symptoms between a few days to a week is the typical time course. However, the symptoms can recur sooner and with more severity with repeated subsequent exposures.² After the appropriate diagnosis of fixed drug eruption, this patient’s PCP prophylaxis was switched to atovaquone, trimethoprim/sulfamethoxazole was added to his drug allergy list, and triamcinolone 0.1% ointment alleviated symptoms of pruritus.

Incorrect Options

1. Describes histopathology of lichen planus,³ which would typically have clusters of smaller papules and plaques rather than the larger ovoid thin plaques seen with this patient. Drug-induced lichen planus/lichenoid drug eruption can be considered with multiple anti-hypertensives in the clinical history. Although histopathology can resemble typical lichen planus, the distinguishing feature can be the presence of increased eosinophils.
2. Describes histopathology of Kaposi sarcoma,³ which would be a reasonable morphological consideration in the setting of immunocompromise with a CD4 count <200. However, the multiple circular and ovoid plaques, in the context of a classic medication offender, are more likely fixed drug eruption, which was confirmed on biopsy for this patient.
3. Describes histopathology of lichen planus pigmentosus,⁴ which would typically be more confluent and present more commonly on sun-exposed areas.
4. Describes histopathology of tinea corporis,³ which would typically appear more annular and ill-defined rather than so well-demarcated and homogenous throughout the plaque. 

References

1. Elston DM. Chapter 7 – Interface dermatitis. In: Dermatopathology. 3^rd Elsevier; 133-152.
2. Bergqvist C, Ingen-Housz-Oro S, and Chosidow O. Chapter 21 – Drug Reactions. In: Dermatology. 5th Edition. Elsevier; 355-384.
3. Elston DM. Dermatopathology. 3^rd Elsevier.
4. Vega ME, Waxtein L, Arenas R, Hojyo T, Dominguez-Soto L. Ashy dermatosis and lichen planus pigmentosus: a clinicopathologic study of 31 cases. Int J Dermatol. 1992 Feb;31(2):90-4. PMID: 1559749.

June 2025 Case Study

Author: Alexis E. Carrington, MD
Reviewed by: Anna Yasmine Kirkorian, MD

A 5-month-old male with no significant medical history presents with a 3-month history of a generalized pruritic rash. The eruption began on the feet and spread upward. The patient’s mother reports significant sleep disruption due to itching. He failed oral valacyclovir and topical desonide previously prescribed. The patient’s mother and sister also developed pruritic rashes.

On examination, the patient had generalized inflammatory nodules and pustules, most prominent on the axillae, trunk, nape of the neck, and lateral feet.

Which of the following is the most appropriate initial diagnostic test for this patient?

Image 1: Many scattered erythematous-violaceous nodules extending from the left inner arm to the trunk.

Image 2: Several scattered pustules and inflammatory nodules on the lateral and dorsal left foot.

Image 3: Positive mineral oil prep demonstrating a live scabies mite and scybala.

A) Skin mineral oil preparation
B) Bacterial culture
C) Skin biopsy for histopathology
D) Fungal culture

Correct Answer: A) Skin mineral oil preparation
A mineral oil prep is the first-line, rapid, and inexpensive test to diagnose scabies by directly visualizing mites, eggs, or scybala under the microscope. Skin biopsy and cultures may be considered if the diagnosis remains uncertain after initial evaluation but are not the first step when scabies is strongly suspected based on clinical findings.

This patient has scabies confirmed by positive mineral oil prep. Scabies is caused by infestation with the mite Sarcoptes scabiei and presents with intensely itchy papules, nodules, and burrows, often worsening at night. Scabies is highly contagious via skin-to-skin contact and fomites.^1,2 Scabetic nodules on the trunk, axillae and genitalia are the most common presentation in infants and can remain for several months after resolution.³

A skin mineral oil preparation (Choice A) is the most appropriate and efficient initial diagnostic test for confirming scabies by directly visualizing mites, eggs, or scybala under the microscope. A bacterial culture (Choice B) would only detect secondary bacterial infections, such as impetigo from scratching, and would not diagnose the underlying scabies infestation. A skin biopsy (Choice C) could potentially reveal mites or burrows under histopathology, but it is more invasive, time-consuming, costly, and less sensitive early in the disease. A fungal culture (Choice D) would be reasonable if considering deep fungal infections like coccidioidomycosis or cryptococcosis, but would be less likely to be seen in an immunocompetent patient.

All household members should be treated simultaneously to prevent reinfestation, and thorough cleaning of bedding, clothing, and fomites is crucial.

References:

1. Bolognia, Jean L. Dermatology. 4th ed. Elsevier, 2018.
2. James WD, Berger TG, et al. Andrews’ Diseases of the Skin: Clinical Dermatology. 13th ed. Elsevier, 2019.
3. Paller AS, Mancini AJ. Cutaneous disorders of the newborn. In: Paller AS, Mancini AJ, eds. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood & Adolescence. 6th ed. St. Louis, Missouri: Elsevier; 2021.

May 2025 Case Study

Author: Dillon Nussbaum, MD¹

1. Department of Dermatology, George Washington University School of Medicine and Health Sciences

Patient History

A 42-year-old man presents with several well-demarcated, erythematous plaques with central atrophic hypopigmentation, peripheral hyperpigmentation, and adherent scale on his scalp, back, and cheeks for several months (Figure 1). He notes mild pruritus and hair loss in the affected areas but denies systemic symptoms. A punch biopsy is obtained and is significant for interface dermatitis and mucin deposition.

Which of the following ophthalmologic findings may develop in a small percentage of patients taking the first-line systemic therapy for this condition longitudinally?

Correct Answer: C

Explanation/Literature Review:

Histopathologic findings of interface dermatitis and mucin deposition along with clinical findings of atrophic hypopigmented plaques with peripheral hyperpigmentation are consistent with a diagnosis of discoid lupus erythematosus (DLE).¹ The first-line systemic agent for widespread or refractory DLE is hydroxychloroquine, which inhibits Toll-like receptors 7 and 9 and downregulates the interferon mediated inflammatory cascade implicated in DLE. Although generally well-tolerated, hydroxychloroquine carries a risk of retinal toxicity, particularly with long-term use or dosing above 5 mg/kg/day. Hydroxychloroquine accumulates in the retinal pigment epithelium and can cause a central scotoma, which presents as a focal blurry or blind spot at the center of the visual field, and is typically irreversible. Studies indicate the incidence of central scotoma in patients taking hydroxychloroquine ranges from 0.5% to 7.5% after 5 years of therapy, with most cases being mild, and the variability depending on diagnostic criteria. Baseline and annual ophthalmologic exams, including visual field testing and optical coherence tomography, are recommended after 5 years of therapy or earlier in higher-risk patients.^2-4

DLE commonly occurs in sun exposed areas with a predilection for the conchal bowls, often resolves with scarring and alopecia, and is worsened by tobacco use. Topical therapies include corticosteroids and non-steroidal anti-inflammatory agents in addition to daily photoprotection. Hydroxychloroquine is first line for both systemic lupus erythematosus (SLE) and DLE and other systemic immunosuppressants are frequently used in conjunction with hydroxychloroquine when appropriate. Janus kinase inhibitors are increasingly being utilized off label for both DLE and SLE. While uncommon, DLE can be associated with SLE, and if so, monoclonal antibodies such as belimumab or anifrolumab can be utilized.^5,6 Incorrect answers include Kayser-Fleischer rings, which are dark copper colored rings on the periphery of the iris seen in Wilson’s disease. Cataracts, or clouding of the lens, is associated with corticosteroid use among other etiologies, but has not been associated with the use of hydroxychloroquine. Retinal detachment and optic neuritis are unrelated to hydroxychloroquine use.

References:

1. McDaniel B, Sukumaran S, Koritala T, et al. Discoid Lupus Erythematosus. [Updated 2023 Aug 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
2. Ahn S. J. (2024). Classification of Hydroxychloroquine Retinopathy: A Literature Review and Proposal for Revision. Diagnostics (Basel, Switzerland), 14(16), 1803.
3. Marshall, E., Robertson, M., Kam, S., Penwarden, A., Riga, P., & Davies, N. (2021). Prevalence of hydroxychloroquine retinopathy using 2018 Royal College of Ophthalmologists diagnostic criteria. Eye (London, England), 35(1), 343–348.
4. Melles, R. B., Jorge, A. M., Marmor, M. F., Zhou, B., Conell, C., Niu, J., McCormick, N., Zhang, Y., & Choi, H. K. (2023). Hydroxychloroquine Dose and Risk for Incident Retinopathy : A Cohort Study. Annals of internal medicine, 176(2), 166–173.
5. Abduelmula, A., Sood, S., Mufti, A., Hinek, A., & Yeung, J. (2023). Management of cutaneous lupus erythematosus with Janus kinase inhibitor therapy: An evidence-based review. Journal of the American Academy of Dermatology, 89(1), 130–131.
6. Merola, J. F., Prystowsky, S. D., Iversen, C., Gomez-Puerta, J. A., Norton, T., Tsao, P., Massarotti, E., Schur, P., Bermas, B., & Costenbader, K. H. (2013). Association of discoid lupus erythematosus with other clinical manifestations among patients with systemic lupus erythematosus. Journal of the American Academy of Dermatology, 69(1), 19–24.

April 2025 Case Study

Author: Nikita Menta, BA¹, Nidhi Shah, MD¹, Karl Saardi, MD¹

1. Department of Dermatology, The George Washington University School of Medicine and Health Sciences

Patient History
A 43-year-old female presented to the clinic with several painful, erythematous, edematous plaques in addition to hyperpigmented plaques on the arms and legs, which had been present for more than 24 hours. The rash initially started about four years prior to presentation and was unresponsive to a variety of oral antihistamines and a four-month trial of omalizumab. The patient also endorsed intermittent episodes of angioedema as well as occasional low back and knee pain. She previously underwent a punch biopsy on the lower left back; hematoxylin and eosin staining demonstrated marked dermal edema, margination of neutrophils with perivascular and interstitial infiltrate including eosinophils, perivascular nuclear debris with neutrophils, and significant extravasation of erythrocytes. Exam findings are shown in Figure 1.

Based on the clinical presentation and biopsy findings, which of the following laboratory tests would be most useful in determining the prognosis of this condition?

A) Antinuclear antibodies
B) Erythrocyte sedimentation rate
C) Complement Levels
D) C-reactive protein
E) Liver function tests
F) Rheumatoid factor
G) Antithyroid antibodies

Correct Answer: C

Explanation/Literature Review:
This patient’s treatment-resistant urticarial plaques combined with histopathologic findings demonstrating perivascular nuclear debris with neutrophils and extravasation of erythrocytes are consistent with a diagnosis of urticarial vasculitis (UV). UV classically presents as recurrent, long-lasting wheal-like lesions with a predilection for the trunk and proximal extremities, accompanied by histopathologic findings of leukocytoclastic vasculitis.¹ UV can present with or without angioedema. Additionally, features that help distinguish UV from chronic spontaneous urticaria (CSU) include the persistence of lesions beyond 24 hours, predominant symptoms of burning and pain compared to pruritus, and residual post-inflammatory purpura or hyperpigmentation upon healing.^2,3 UV is a rare condition with an estimated incidence of 0.5 per 100,000 in the United States.⁴ It most commonly occurs in individuals in their 5^th to 7^th decades of life and demonstrates a female gender predominance.⁵ Regarding pathophysiology, UV is a type III hypersensitivity reaction; however, in most cases, the triggering antigen is often unidentified.⁶ While the majority of UV cases are idiopathic, a small percentage of cases have been associated with medications, infectious diseases, malignancies, and autoimmune diseases, commonly systemic lupus erythematosus.²

There are two main subtypes of UV, which are classified based on complement levels, the most important indicator of UV prognosis (answer choice C). Patients with normal complement levels, or normocomplementemic UV (NUV), tend to have skin-limited vasculitis. Conversely, patients with low complement levels, or hypocomplementemic UV (HUV), are much more likely to experience systemic disease.^1,2 The most common systemic manifestations of HUV include arthralgia, arthritis, inflammatory eye diseases, pulmonary symptoms (mimicking asthma or COPD), gastrointestinal symptoms, and renal pathologies (proteinuria/hematuria).¹ Finally, there is also a more severe subtype of HUV, called HUV syndrome (HUVS), which is defined by multiorgan involvement.¹

UV is a notoriously challenging condition to treat, further complicated by the lack of standardized guidelines and randomized controlled trials. In a recent review article, H1-antihistamines, omalizumab, and immunomodulators were among the treatments with the most robust evidence in UV management.^4,7 However, while H1-antihistamines were widely employed, they were only effective in improving skin lesions in 9.9% of 141 patients.⁷ Omalizumab demonstrated much greater efficacy, with 76% of 108 patients experiencing improvement in cutaneous symptoms and many also experiencing improvement in systemic symptoms such as arthralgia and abdominal pain.⁷ Among immunomodulators, systemic corticosteroids, dapsone, and hydroxychloroquine had the most substantial and strongest evidence supporting their use in addressing cutaneous and systemic symptoms of UV; however, the potential adverse effects of these drugs must be carefully considered.^4,7 The aforementioned review article proposed a treatment algorithm recommending that mild UV should be approached like CSU, starting with H1-antihistamines and escalating to omalizumab, whereas moderate-to-severe UV should be managed with corticosteroids and/or other immunomodulatory agents depending on the patient profile.⁷ While this algorithm offers some direction, there is a critical need for high-quality, head-to-head trials to determine the optimal approach to UV management.

Incorrect answer choices:
The other laboratory tests are not indicative of prognosis but are warranted in the workup of patients with UV, particularly HUV. Inflammatory markers, specifically erythrocyte sedimentation rate (B) and C-reactive protein (D), are typically elevated in UV.^1,5 Additionally, since UV can be associated with autoimmune diseases, autoimmune laboratory tests, including but not limited to antinuclear antibodies (A), rheumatoid factor (F), and anti-thyroid antibodies (G) are often included in the workup to detect or rule out underlying autoimmune diseases.⁵ Finally, while liver dysfunction is not a common systemic manifestation of UV, liver function tests (E) may be included alongside standard laboratory tests, such as complete blood count and basic metabolic panel, in the workup of UV.⁵ 

References

1. Marzano AV, Maronese CA, Genovese G, et al. Urticarial vasculitis: Clinical and laboratory findings with a particular emphasis on differential diagnosis. J Allergy Clin Immunol. 2022;149(4):1137-1149. doi:10.1016/j.jaci.2022.02.007
2. Bolognia J, Schaffer JV, Cerroni L, Callen JP. Dermatology. Elsevier; 2025.
3. James W. Andrews’ Diseases of the Skin. Elsevier; 2026.
4. Kolkhir P, Grakhova M, Bonnekoh H, Krause K, Maurer M. Treatment of urticarial vasculitis: A systematic review. J Allergy Clin Immunol. 2019;143(2):458-466. doi:10.1016/j.jaci.2018.09.007
5. Wang RX, Newman SA. Urticarial Vasculitis. Immunol Allergy Clin North Am. 2024;44(3):483-502. doi:10.1016/j.iac.2024.03.006
6. Black AK. Urticarial vasculitis. Clin Dermatol. 1999;17(5):565-569. doi:10.1016/s0738-081x(99)00062-0
7. Rothermel ND, Vera Ayala C, Gonçalo M, et al. Managing Urticarial Vasculitis: A Clinical Decision-Making Algorithm Based on Expert Consensus. Am J Clin Dermatol. 2025;26(1):61-75. doi:10.1007/s40257-024-00902-y